Flashcards in Cell to Cell Communication Deck (21)
How do skeletal muscle fibres contract and relax?
Contract when Ach is released at neuromuscular junction
Relax when the alpha-motor neurone itself is inhibited as skeletal muscle fibres only receive one input directly (Ach)
What factors increase the speed of AP propagation?
- Larger axon diameter
- More myelinated axon
What is the neuro pathology of Multiple Sclerosis?
- LOSS of MYELIN
- Plaques occur anywhere in CNS white matter
- Slows, delays or blocks AP transmission
- producing sensory, motor, cognitive or behavioural deficits
Describe the two synapse types
--> cardiac function (gap junctions), present in NS, unclear role
--> majority, many roles using many NTs, therapeutically VERY relevant
What are the 4 steps in terms of the life of a neurotransmitter?
Describe the 2 types of NT synthesis and therapeutic relevance
1. Synthesis in the cell body (eg. neuropeptides)
2. Local synthesis (eg. catecholamines) (tyr -> l-dopa -> dopamine, NA)
eg. Parkinson's - L-DOPA enzyme increased to produce more dopamine
(dopamine involved in mood, memory, movement, attention etc)
Describe NT release and therapeutic relevance
- action potential arrives at terminal bouton
- activates VGCCs
- no calcium inside cell, high outside cell so Ca INFLUX
- Calcium binds to vSNARE + tSNARE proteins
- triggers fusion, exocytosis
eg. Botulinum toxin blocks neuromuscular transmission by interfering with Calcium release
What are some features of post-synaptic receptors?
1) excitatory or inhibitory
2) fast (ligand gated/iono) or slow (g protein/metabo)
Example and response of ionotropic EXCITATORY receptor
- glutamate in CNS
- Ach @ NMJ
- bind to receptor, cause SODIUM influx -> depolarisation -> EPSP (electrotonic)
Example and response of ionotropic INHIBITORY receptor
- glycine (spinal cord, retina)
- bind to receptor, cause CHLORIDE influx -> hyperpolarisation -> IPSP (electrotonic)
Example and response of metabotropic receptor
- dopamine, ACh, serotonin, NA
- long lasting, involve second messengers, used in MODULATORY pathways
Examples of therapeutic interventions in regards to receptor action?
- Some drugs bind to same site as NT
---> nicotine at ionotropic nicotinic Ach receptors
---> curare blocks neuromuscular Ach receptors
- Some drugs bind to other sites on receptor, to modify response to NT
---> benzodiazepines enhance effect of GABA at GABA receptors
---> strychnine reduces effect of glycine at glycine receptors
Discuss types and examples of neurotransmitter removal
1) DIFFUSION - peptides
2) ENYMATIC degradation - AChE (inhibitors of this will inc cholinergic transmission)
3) RE-UPTAKE - dopamine, NA, serotonin
4) GLIAL UPTAKE - glutamate, GABA (by astrocytes - for fast transmitters)
What is the action of cocaine?
Blocks re-uptake of dopamine into pre-synaptic membrane, resulting in a greater 'reward' feeling.
How is hypoxia linked to glutamatergic toxicity?
- uptake of glutamate requires oxygen
- in hypoxic conditions (eg stroke), glutamate remains in the cleft
- toxic effect as it builds up
Discuss the negative feedback displayed during synaptic transmission
- presynaptic receptors bind NT released by cell, reduce amount of NT released with each AP, tones things down - site for drugs
- post synaptic receptors send RETROGRADE signals to decrease NT release
What's a gr8 saying by P.Murphz?
cells that fire together, wire together x
What is long-term potentiation?
When useful synapses are strengthened - increased plasticity
What 4 things happen to strengthen a synapse?
- more receptors
- receptor function improved
- more transmitter made
- more transmitter released
How are memories formed?
Secondary messengers from activation of metabotropic receptors enhance long-term potentiation process.